Lim C-M, Hong S-B, Koh Y, Lee S D, Kim W S, Kim D-S, Kim W D
Division of Respiratory and Critical Care Medicine, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 138-600.
Lung. 2003;181(1):23-34. doi: 10.1007/s00408-002-0111-x.
Alveolar hemorrhage and pulmonary edema induced by mechanical ventilation are partly dependent on cardiac output. Because cardiac output is low during hypothermia, we hypothesized that hypothermia may protect against these vascular manifestations of ventilator-induced lung injury. Twenty-seven Sprague-Dawley rats were assigned to either normothermia (37 +/- 1 degrees C)-injurious ventilation (NT; n = 10), hypothermia (27 +/- 1 degrees C)- injurious ventilation (HT; n = 10), or nonventilated control ( n = 7). The two ventilated groups were subjected to injurious ventilation of peak airway pressure 30 cm H(2)O with zero end-expiratory pressure for 20 min. Compared with the NT group, the hemorrhage/congestion score of the lung (11.2 +/- 1.5 vs. 4.7 +/- 1.6; p < 0.001) and the ratio of wet/dry lung weight (6.1 +/- 0.8 vs. 5.0 +/- 0.1; p = 0.046) of the HT group were lower. Compared with the NT group, protein concentration (3,471 +/- 1,985 micro g/ml vs. 1,374 +/- 726 micro g/ml; p = 0.003) and lactate dehydrogenase level (0.43 +/- 0.22 U/ml vs. 0.18 +/- 0.1 U/ml; p = 0.046) in bronchoalveolar lavage fluid of the HT group were lower. Whereas pressure-volume curve was shifted to the right in the NT group after injurious ventilation, it was not shifted in the HT group. In conclusion, hypothermia in rats attenuated the degrees of vascular manifestations and alveolar epithelial injuries induced by injurious ventilation, and preserved the mechanical properties of the lung.
机械通气引起的肺泡出血和肺水肿部分取决于心输出量。由于低温时心输出量较低,我们推测低温可能预防呼吸机诱导的肺损伤的这些血管表现。将27只Sprague-Dawley大鼠分为正常体温(37±1℃)-损伤性通气组(NT;n = 10)、低温(27±1℃)-损伤性通气组(HT;n = 10)或非通气对照组(n = 7)。两个通气组接受气道峰值压力30 cm H₂O、呼气末压力为零的损伤性通气20分钟。与NT组相比,HT组肺出血/充血评分(11.2±1.5对4.7±1.6;p < 0.001)和肺湿/干重比(6.1±0.8对5.0±0.1;p = 0.046)较低。与NT组相比,HT组支气管肺泡灌洗液中的蛋白质浓度(3471±1985 μg/ml对1374±726 μg/ml;p = 0.003)和乳酸脱氢酶水平(0.43±0.22 U/ml对0.18±0.1 U/ml;p = 0.046)较低。损伤性通气后,NT组压力-容积曲线右移,而HT组未右移。总之,大鼠低温可减轻损伤性通气诱导的血管表现和肺泡上皮损伤程度,并保留肺的力学性能。